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Tumor lipids were studied in the experimental model Human Lung Carcinoma/nude mice as well as the effect of this human neoplasm on the host liver lipid metabolism. Fatty acid profiles from tumoral lipids revealed the loss of specificity for fatty acid composition in triglycerides. Host liver fatty acid composition and cholesterol metabolism were affected by the implanted human lung tissue. A noticeable increase ratio between saturated/unsaturated fatty acids was observed in host liver fatty acid phospholipids (1.17 +/- 0.17) in comparison to control liver (0.84 +/- 0.04). Cholesterol synthesis was assessed "in vivo" by means of [14C]acetate incorporation. The specific radioactivity of [14C] cholesterol was increased by a factor of about 6 in host liver as compared with control liver. This observation along with the marked decrease in the cholesterol content of host liver and the hypocholesterolemia detected in the host mice led us to suggest an increase in the liver cholesterol catabolism promoted by the presence of the tumor.

The effect of normal or sensitized spleen cell transfer from syngeneic euthymic mice to Junin virus-infected suckling athymic mice was studied. Transfer was performed 1 or 7 days after infection. In both cases, an acute lethal disease developed 6-11 days after transfer. The mortality reached 100% in all infected groups receiving normal or sensitized splenocytes, while it was negligible for different control groups of athymic mice. Transfer of normal or sensitized splenocytes was unable to significantly modify brain viral titers, as compared with infected nontransferred athymic mice killed after a 25-day observation period. Brain lesions were demonstrated in about half of the infected athymic mice transferred with sensitized splenocytes and in all euthymic infected mice. These results show that splenocyte transfer from immunocompetent donors is able to change the normal course of persistent Junin virus infection in nude mice to a lethal acute disease, thus pointing to a main role for T cells in its pathogenesis.

Splenocytes from Junin-virus-persistently-infected euthymic mice taken at 45 days postinfection seemed unable to induce overt signs of disease, to cause death, or to modify brain viral levels when transferred to athymic Junin-virus-infected mice. Findings differed sharply when the same recipients were transferred with splenocytes taken at 6 or 30 days postinfection from immunocompetent mice infected in adult life, since mortality reached 80 or 50%, respectively, and brain viral titers were significantly lowered. Furthermore, splenocytes taken at 6 days postinfection from whole adult mice proved harmless to persistently infected euthymic mice. These findings strongly suggest the existence of an immune system alteration in the immunocompetent mouse, attributable to Junin virus persistence. This premise is based on the fact that splenocytes from persistently infected mice were unable to recognize viral antigen expressed on recipient-infected cells. The absence or impairment of a specific cytotoxic T cell population is hereby postulated.